AbstractThe ability of B lymphocytes to process and present antigen to helper T cells is essential to initiate T cell‐B cell interactions in humoral immune responses. Here we describe the developmental acquisition of the antigen‐presenting function of B cells as measured by the ability of B cells to stimulate a T cell hybrid to interleukin (IL)‐2 secretion. Neonatal splenic B cells are not adult‐like in their ability to process and present the model protein antigen pigeon cytochrome (Pc), which enters the B cell through fluid‐phase pinocytosis, until 21 to 28 days of life. The ability of neonatal B cells to process and present antigen which enters the cell bound to surface Ig is not adult‐like until 28 days of age. When neonatal B cells acquire antigen‐presenting cell (APC) function, surface IgM facilitates antigen processing. The delayed acquisition of APC function cannot be accounted for solely by a deficiency in major histocompatibility complex MHC class II, ICAM‐1, or LFA‐1 as neonatal B cells express adult levels of these molecules by 7–14 days after birth. Moreover, the ability of neonatal B cells to present a peptide fragment of Pc which does not require processing is adult like by day 14. Furthermore, neonatal B cells are capable of binding, internalizing and degrading radiolabeled antigen, suggesting a more subtle level of regulation. In contrast to neonatal B cells, immature B cells in the adult bone marrow and adult B cells undergoing antigen‐driven differentiation to memory B cells, as defined by the loss of the J11D marker, are competent to process and present antigen resulting in T cell IL‐2 secretion. Thus, developing B cell subpopulations in the adult and in the neonate can be distinguished. Only neonatal B cells are deficient in their ability to stimulate T c
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